Keywords

Introduction

Following SAH a massive diuresis, natriuresis and hyponatraemia may occur, termed 'cerebral salt wasting'. The aetiology of this condition is unclear and its existence has been questioned [1,2]. This study aimed to document sodium balance in a patient cohort treated by the same protocol following SAH, hoping to further elucidate the mechanism of this condition.

Patients and methods

Prospectively entered data from a computerised database of SAH patients admitted to an eight-bedded neurosurgical ICU were analysed to assess the correlation of sodium flux with the course of the disease. For up to 18 consecutive days plasma sodium was measured, 24-hour urinary collections were analysed for sodium loss and the daily intravenous sodium intake was calculated from the charted intravenous fluids.

Patients underwent check cerebral angiography on day 5-7 following admission or earlier if there was clinical evidence of vasospasm. Papaverine was administered to patients with vasospasm who then underwent further angiography and hypertensive therapy with noradrenaline. The total doses of papaverine and noradrenaline administered were used as markers of the severity of spasm.

Results

Data from 39 patients was analysed. In 15 patients urinary sodium excretion and hence sodium balance could be calculated for 8 or more days. The median sodium input was 360 mmols/day (range 15-4868), see Figures for daily plasma sodium and sodium balances.

Measured sodium balance was consistently negative in this population. There were no significant differences between high and low papaverine and noradrenaline groups.

Figure

Conclusions

In this limited dataset, following SAH and saline loading, plasma sodium increased in these patients but there was no obvious natriuretic phase. Cerebral salt wasting was not clearly demonstrated by these data.